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Biomedical subjects

J Gueris

Publications and source records attributed to J Gueris.

At least 19 recordsLinked to original sources
PubMed1991

Comparison of intact, midregion, and carboxy terminal assays of parathyroid hormone for the diagnosis of bone disease in hemodialyzed patients.

The predictive value of three different RIAs of PTH for the diagnosis of the histological type of bone disease has been compared in 24 asymptomatic patients on chronic hemodialysis who had never been exposed to aluminum intoxication and who agreed to have a bone biopsy after double tetracycline labeling. The serum concentrations of PTH were measured using a two-site immunoradiometric assay for intact PTH(1-84) and region specific assays directed against the C-terminal (53-84) fragment or the midregion (44-68) of the molecule. The bone histomorphometric analysis showed that six patients had nonaluminic adynamic bone disease with low bone formation rate (BFR), eight had mild hyperparathyroidism characterized by increased bone resorption and normal BFR, nine had severe hyperparathyroidism with increased BFR, and only one had true osteomalacia with increased osteoid seam thickness. All PTH assays correlated with the various parameters of bone resorption and bone formation and were able to differentiate the histological type of bone disease only when groups of patients were considered. For classifying individual patients into severe hyperparathyroidism and adynamic bone disease groups, the intact PTH assay had the best predictive value with a sensitivity of 100% and a specificity of at least 70%. A nonaluminic adynamic bone disease was observed in more than 50% of the patients who had normal intact PTH levels (6/11). It is concluded that the intact PTH measurement is superior to C-terminal and midregion assays for the prediction of the histological type of bone disease in hemodialyzed patients and should be of considerable value to adapt their treatment in order to avoid the emergence of both severe hyperparathyroidism and adynamic bone disease. In the absence of aluminum intoxication it seems that maintaining intact PTH concentrations 1 to 1.5 times the upper limit of normal would correspond to the best bone histology.

Bone Diseases↗
PubMed1991

Parathyroid hormone related protein (PTHrP) and breast cancer.

PTHrP, a newly characterized peptide is responsible for humoral hypercalcemia of malignancy in squamous cancers. It is also expressed by a variety of normal tissue and might have growth factor propriety. It is expressed by lactating breast and is frequently present in breast cancer. Although it is responsible for humoral hypercalcemia in an animal model of breast cancer its role in breast cancer hypercalcemia is still putative. The possibility that it might be one of the autocrine growth factors implicated in breast cancer cell proliferation has been suggested.

Animals↗
PubMed1979

[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)].

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.

Adult↗
PubMed1978

[Immobilisation hypercalcaemia. 1 case (author's transl)].

A 21-year-old man suffered severe (up to 15.5 mg%) and prolonged (7 months) hypercalcaemia as a result of immobilisation following severe trauma. During the period of hypercalcaemia, plasma parathormone and calcitonin levels were undetectable. A study using radioactive calcium revealed a very marked increase in bone resorption, a moderate increase in accretion and virtually no intestinal absorption. Iliac biopsy revealed dense calcification front and there was no osteoid substance. This hypercalcaemia appeared to be due to increased bone resorption, while the synthesis of osteoid substance seemed to be insufficient to permit an equivalent increase in calcium accretion.

Adult↗
PubMed1978

[The estimation of parathormone in primary hyperparathyroidism (author's transl)].

In a recent series of 110 cases of primary hyperparathyroidism, estimations of plasma immuno-parathormone (PTH) were carried out in fifty two patients. This estimation proved reliable, making possible the confirmation of the diagnosis. In the absence of renal insufficiency, there was a highly positive relationship between PTH levels and plasma calcium. The relationship between PTH and the weight of the parathyroid tumour was less significant. For technical reasons, this long and difficult estimation cannot be used on a routine basis. However, it is most useful in cases in which other laboratory findings are not typical.

Adenoma↗
PubMed1978

The effect of 1alpha(OH)D3 and 1alpha,25(OH)2D3 on the bone in patients with renal osteodystrophy.

Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.

Aged↗
PubMed1978

Vitamin D metabolites and bone mineralization in man.

A comparison was made of the biochemical and osseous effects of 25-hydroxyvitamin D3 [25(OH)D3], 1 alpha-25-hydroxyvitamin D3 [1 alpha, 25(OH)2D3], and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in adult vitamin D-deficient man. Administration of 50 micrograms/d of 25(OH)D3 for 8 weeks led to a return of the mineralization front to normal associated with a return of TmPO4/GFR to normal, an increase in serum phosphate and calcium concentrations, a fall in serum IPTH, and a rise in serum alkaline phosphatase activity. Giving 2.5 micrograms/d of 1 alpha,25(OH)2D3 did not produce these effects. Administration of 1 alpha, 25 (OH)2D3 caused an increase in intestinal calcium absorption, and a rise in serum calcium associated with a fall in serum immunoreactive parathormone (IPTH) concentrations but no sustained rise in either alkaline phosphatase, serum phosphate concentration, nor in TmPO4/GFR. Its administration caused an increase in the extent of the osteoclastic bone resorption surface but the extent of the mineralization front remained subnormal. Administration of 20 micrograms/d of 24,25(OH)2D3 caused a fall in urinary calcium excretion and in serum IPTH, and a rise in serum alkaline phosphatase, but no change in TmPO4/GFR or serum phosphate, and only a slight increase in the extent of the mineralization front. Combined treatment with 1 alpha, 25(OH)2D3 and 24,25(OH)2D3 led to a return of the mineralization front of normal even though both TmPO4/GFR and serum phosphate concentration remained low. It is concluded that 1alpha,25(OH)2D3 is not the sole biologically active metabolite of vitamin D in man. It is apparent that either 25(OH)D3 or some as yet unidentified metabolite of 25(OH)D3 stimulates the renal tubular reabsorption of calcium and phosphate, and that the subsequent rise in serum phosphate concentrations along with the direct actions of 1 alpha-25(OH)2D3, 24,25(OH)2D3, and possibly 25(OH)D3 on bone cells all participate in the restoration of normal bone formation and bone mineralization in vitamin D-deficient man.

Alkaline Phosphatase↗
PubMed1978

[Effects of the main derivatives of vitmain D in 3 siblings with "pseudo-deficiency" rickets].

Three siblings, respectively 20, 16 and 12 years old, presented with hypocalcemic vitamin D resistant rickets (Prader's type). Their clinical history included several periods of spontaneous cessation of therapy, with severe relapses. Since 1973, treatment was strictly observed, allowing to test the therapeutic effects of 25 OH D3, 1-25 (OH) 2 D3 and 1-alpha (OH) D3. The clinical effects are reported as well as biochemical data. Among them, an inactive form of hyperparathyroidism is emphasized, which may resemble some cases of pseudohypoparathyroidism. Simultaneous resistance to exogenous PTE was also demonstraded.

Adolescent↗
PubMed1978

[Current data on prolactin].

Prolactin has been lately singled-out among the pituitary hormones, and as such the object of considerable research in the past 15 years. The frequency of prolactin secreting adenomes is established now. The responsibility of iatrogenic factors (neuroleptics, oral contraceptives) in some hyperprolactinaemias is a known fact. The study of the inhibiting dopaminergic system was a landmark in the treatment of hyperprolactinaemia. During the recent Nice Congress, some issues remained unsettled on the physiological activities of prolactin. The matter is clearer when it comes to prolactin secretion. In equilibrium between inhibiting and stimulant factors, the secretion is controlled by the CNS, influenced by the hormonal environment, and its timing is the object of a retrocontrol. This is a very instructive pattern in endocrinology.

Animals↗
PubMed1977

[The relationship between parathormone and calcium blood levels in primary hyperparathyroidism. Diagnostic value (authors transl)].

The results of radio-immunoassay of parathormone in peripheral venous blood (using an anti-serum preferentially recognising fragments from the carboxyl-terminal pole) were compared with those of blood calcium measured on the same day in 33 cases of primary hyperparathyroidism. In the 28 patients with hypercalcaemia, PTH was invariably high (27 cases) or at the upper limit of normal (1 case). In the 5 patients with normal blood calcium levels, it was normal in 3 cases. It is thus important to take blood calcium levels into account in the interpretation of PTH estimation, that latter being more valid during a hypercalcaemic phase.

Calcium↗